Abstract
Merkel cell polyomavirus (MCPyV) infection causes near-ubiquitous, asymptomatic infection in the skin, but occasionally leads to an aggressive skin cancer called Merkel cell carcinoma (MCC). Epidemiological evidence suggests that poorly controlled MCPyV infection may be a precursor to MCPyV-associated MCC. Clearer understanding of host responses that normally control MCPyV infection could inform prophylactic measures in at-risk groups. Similarly, the presence of MCPyV in most MCCs could imbue them with vulnerabilities that-if better characterized-could yield targeted intervention solutions for metastatic MCC cases. In this review, we discuss recent developments in elucidating the interplay between host cells and MCPyV within the context of viral infection and MCC oncogenesis. We also propose a model in which insufficient restriction of MCPyV infection in aging and chronically UV-damaged skin causes unbridled viral replication that licenses MCC tumorigenesis.
Highlights
Merkel cell polyomavirus (MCPyV) infection can be detected on the skin of most healthy adults (Tolstov et al, 2009; Schowalter et al, 2010), yet details of its virology and infectious cycle remain sparse
To take steps in establishing the cellular context of MCPyV infection, we discovered that primary human skin dermal fibroblasts support productive MCPyV infection in vitro and ex vivo (Liu et al, 2016b)
After establishing the MCPyV gene expression and replication kinetics in infected cells, we found that late events in the infectious cycle activated the cGAS-STING and NF-κB pathways and subsequent expression of anti-viral interferon-stimulated genes (ISGs) as well as innate inflammatory cytokines (Krump et al, 2021)
Summary
Merkel cell polyomavirus (MCPyV) infection can be detected on the skin of most healthy adults (Tolstov et al, 2009; Schowalter et al, 2010), yet details of its virology and infectious cycle remain sparse. In virus-associated MCC, MCPyV DNA is integrated into the tumor cell genome in a manner that preserves expression of MCPyV genes called tumor (T) antigens (Shuda et al, 2008, 2011; Cheng et al, 2013).
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